Previous work concerning the etiological basis of seizures has led to the concept that monoamine levels in brain tissue regulate seizure susceptibility. This concept has been generally accepted because reserpine and other compounds which decrease concentration of amines in brain are found to increase susceptibility to seizures, whereas compounds which increase concentration of brain 5-hydroxytryptamine, norepinephrine, or dopamine tend to decrease susceptibility. We believe that the major problem in research on seizures is not the seizure itself but the biochemical alterations of the brain leading to the convulsion. It is apparent that artificially induced seizures cannot contribute much to the solution of this problem unless methods are employed to follow cerebral metabolism immediately prior to the seizure and to follow the consequences of the induced seizure on cerebral metabolism of monoamines. We have methods to do this. Our hypothesis is that seizure activity is a result of a change in the balance of monoamine metabolism in brain tissue. Our method of repeated sampling of cerebrospinal fluid represents a new approach to the study of convulsions and monoamine metabolism. With it we can follow changes in the concentrations of the major monoamine metabolites preceding and following a seizure in the same animal. Also, using sub- convulsive and convulsive doses of the seizure-inducing agent, we will be able to differentiate between the effects of the seizure-inducing agent and the convulsion on monoamine metabolism which may provide insight into the cause of convulsive diseases.